Campylobacter concisus is prevalent in the gastrointestinal tract of patients with microscopic colitis

Abstract

Objectives

Microscopic colitis (MC) is potentially induced by an inflammatory reaction to a luminal gut factor. The emerging pathogen Campylobacter concisus is associated with prolonged diarrhoea and subsequently increased risk of MC. We aimed to examine the prevalence of C. concisus in clinical samples from MC patients, analyse the subtypes collagenous colitis (CC) and lymphocytic colitis (LC), and characterise C. concisus isolates from MC patients by genomic sequencing.

Methods

Mucosal biopsies were collected by sigmoidoscopy in 55 MC patients (CC n = 34, LC n = 21). Saliva and faecal samples were also collected. A two-step cultivation method and PCR established C. concisus prevalence. Biopsy and faecal isolates were sequenced for genomic analysis.

Results

Cultivation revealed C. concisus in saliva 55/55, faeces 14/55 and biopsies 69/436, which was confirmed by PCR in faeces 28/55 and biopsies 215/430. Interestingly, biopsy prevalence was higher in CC patients than in LC patients both by cultivation (50/270 vs.19/166, p = .058) and by PCR (175/270 vs. 40/160, p < .0001). Long disease duration also affected biopsy prevalence both by cultivation 30/244 (<2 years) vs. 39/192 (>2 years) (p = .025) and by PCR 103/239 (<2 years) vs. 112/191 (>2 years) (p = .002). Genomic analysis on sixty biopsy and twenty faecal isolates revealed division into two clusters/genomospecies and a high presence of various, putative virulence genes (zot, exotoxin 9 and hcp).

Conclusions

Campylobacter concisus was prevalent in MC patients. Interestingly, the biopsy prevalence differed in biopsies from CC and LC patients and with regard to disease duration. Further studies are needed to elucidate this possible association.

Keywords:

• Microscopic colitis
• collagenous colitis
• lymphocytic colitis
• Campylobacter concisus
• inflammatory bowel disease
• genomospecies
• virulence genes
• saliva
• stools
• intestinal biopsies

Acknowledgements

The authors would like to thank all patients who volunteered to participate in the study; the medical staff at the Gastroenterology Clinic for help with sigmoidoscopies and biopsy collection; Ditte Helene Lundsted, MSc, for her help in the WGS laboratory; Ihab Bishara Lolas, MSc, PhD, for his help with Sanger verification of PCR products; and Angela Cornelius, MSc, PhD, for her assistance in genomospecies analysis. Part of this study was presented as an abstract online at the 30th International Workshop on European Congress of Clinical Microbiology and Infectious Diseases (ECCMID) 2020.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This work was supported by the Aage og Johanne Louis-Hansens Fond under Grant [19-2B-5096].